Hypoxia And Respiratory Failure Flashcards
What is the difference between hypoxaemia and hypoxia? When would you get hypoxia without hypoxaemia?
Hypoxaemia - low pO2 in blood
Hypoxia - O2 deficiency at tissue level
Hypoxia at tissues without hypoxaemia occurs in anaemia or in poor circulation
What the normal O2 saturation and PaO2?
O2 saturation 94-98%
PaO2 9.3-13.3 KPa
When these levels are below LLN (lower limit of normal) defined as hypoxaemia
When is tissue damage most likely? What is this used to diagnose?
O2 saturation <90%
PO2 <8KPA
This is used to diagnose respiratory failure - the clinical presentation will vary depending if it’s acute or chronic and an arterial blood gas may not always help to distinguish
Causes of hypoxaemia
Low inspired O2 (drowning, high altitudes, hypoventilation (resp pump failure), ventilation/ perfusion mismatch, diffusion defect (problems alveolar capillary membrane), intra-lung shunt (acute respiratory distress syndrome) which is extreme V/Q mismatch, right to left shunt (cyanotic heart disease)
Effects of hypoxaemia
Especially acute:
Impaired CNS function, confusion, irritability, agitation
Cardiac arrhythmias and cardiac ischaemia
Hypoxic vasoconstriction of pulmonary vessels -> pulmonary hypertension -> R heart failure + cor pulmonale (abnormal hypertrophy right heart)
Cyanosis (bluish discolouration of skin and mucous membranes due to presence of 4-6gm/dl of deoxyhaemoglobin)
What are the two types of cyanosis?
Central cyanosis: seen in oral mucosa, tongue, lips indicates hypoxaemia - deoxygenated Hb in arteries <5 g/dl with O2 sats <85%
If ^^ present peripheral cyanosis will also be present
Peripheral cyanosis - fingers, toes, poor local circulation (more O2 extracted by the peripheral tissues)
What occurs in chronic hypoxaemia as mechanisms to increase O2 delivery?
- increased EPOsecreted by kidneys -> raised Hb (polycythemia)
- increased 2,3 DPG shifts Hb saturation curve so O2 released more freely
What’s the definition of type one and two respiratory failures?
Type 1 -Just low O2
low pO2 < 8kpa or O2 saturation <90% room air, PCO2 normal or low, gas exchange impaired at level of alveo-capillary membrane
Can progress to (disease progress and more of lung involved) …
Type 2 - low O2 & high CO2
Low PO2 & high PcO2 >6.5 KPa,
Respiratory pump failure e.g. hypoventilation
Difference: CO2 levels, cause
What determines alveolar ventilation?
(Tidal volume - dead space) X respiratory rate
Which type of respiratory failure would hypoventilation cause and why?
Type 2 as it always causes hypercapnia and hypoxaemia
Causes of hypoventilation
End stage COPD (flattened diaphragm)
Asthma
Stabbing
Drug overdose (suppresses respiratory centre)
Head injury
Neuromuscular disease e.g. muscular dystrophy
End stage pulmonary fibrosis
Obesity (central in Brain or obstructive sleep apnoea and decreased lung space)
Compare acute and chronic hypoventilation
Acute - urgent treatment, may need artificial ventilation, commonest causes: opiate overdose, head injury very severe acute asthma
Chronic - chronic hypoxaemia and hypercapnia, slow progression, time for compensation so better tolerated. Commonest causes: severe COPD, acute exacerbations may occur due to LRT infection
What is scoliosis, kyphosis and kyphoscoliosis? Why can they all cause lung problems?
Scoliosis - sideways curvature of the spine
Kyphosis - XS outward curve results in abnormal rounding of the back ‘hunchback’
Kyphoscoliosis - both
Limit chest space so impaired ability for chest to expand
Causes of respiratory failure
Opiates, head injury, trauma cervical spinal cord, Guillain-Barre syndrome, myasthenia gravis, pneumothorax, v severe acute asthma, foreign body
Causes of chronic type 2 only: myopathy, MD, end stage lung fibrosis, late stages of COPD, kyphoscoliosis
Could be more than one mechanism e..g lung fibrosis -> diffusion defect but if severe hypoventilation also OR pulmonary oedema -> diffusion defect and V/Q mismatch .
Effects of hypercapnia
Respiratory acidosis
Impaired CNS function (drowsiness CO2 narcosis, confusion, coma, flapping tremors arms straight, wrist extended hands flap)
Warm hands, bounding pulse (peripheral vasodilation)
Cerebral vasodilation - headache
Chronic: respiratory acidosis compensates HCO3- kidney, acclimation to CNS effects, vasodilation mild pink puffers
What occurs in central chemoreceptors with chronic CO2 retention?
CO2 diffuses CSF -> PH drops -> stimulates central chemoreceptors -> choroid plexus cells secrete HCO3- in CsF -> CSF PH normal
PCo2 I’m blood still high but central chemoreceptors unresponsive to this ‘reset to a new higher CO2 level’
Now main control is by peripheral chemoreceptors which detect PO2, respiratory drive now driven by hypoxia
How could treatment of hypoxia worsen hypercapnia?
✅ give O2 improves PO2 so peripheral chemoreceptors stop hypoxic respiratory drive (resp rate and depth reduce) -> worsening hypercapnia
And
Correction of hypoxia removes hypoxic vasoconstriction leads increased perfusion of poorly ventilated alveoli and diverts blood away form better ventilated alveoli (V/Q mismatch)
Increasing CO2 May gradual, tel, by increasing blood HCO3-
So need to give controlled O2 therapy target 88-92% and can give ventilatory support
What conditions could cause a V/Q mismatch?
conditions where SoME alveoli are poorly ventilated
O2 therapy
Asthma (variable airway narrowing)
RDS
Pulmonary oedema
Pulmonary embolism
Pneumonia (exudate in affected alveoli)
V/Q = <1 in these alveoli
-> hypoxic vasoconstriction occurs to try to divert some blood to better ventilated alveoli
If this fails..
-> hyperventilation
What’s the final result of hyperventilation caused by a V/Q mismatch on PO2 and PcO2 and why?
Hyperventilation -> affected alveoli still poorly ventilated but unaffected segments increased ventilation:
PO2 rise and pCo2 falls
Increase O2 increased dissolved a little and once HB fully saturated (PO2 >10kPa) has no effect so overall doesn’t compensate for pathological segments
More CO2 dissolves or is transported as HCO3- so doesn’t rely as much on Hb saturation (only 30%)
So final result: low PO2 with normal/ low PCO2 = type one resp failure
Which conditions will lead to a diffusion impairment at alveolar capillary membrane? What does this cause?
Fibrotic lung disease (thickened membrane and interstitium)
Pulmonary oedema (fluid increases diffusion distance)
CO2 less affected as more soluble so: Po2 low and PCO2 normal/ low until end stage = type one respiratory failure
Causes of diffuse lung fibrosis and appearance on spirometry
Causes: idiopathic fibrosing alveolitis, asbestosis, extrinsic allergic alveolitis, pneumoconiosis
Reduced compliance, restrictive lung disease so restrictive pattern on spirometry (reduced FEV1 and FVC reduced on volume, time but no scalloping on expiratory flow rate, volume)
Partially correct hypoxaemia with O2 administration
What is a shunt of the respiratory system? What’s a cause?
Some alveolar are perfused but not ventilated at all e.g. V/Q = 0
Acute respiratory distress syndrome
What is acute respiratory distress syndrome? What does it cause? How can you manage it?
End result of acute alveolar injury caused by different insults e.g. damage to alveolar capillary unit -> increased vascular permeability, oedema, fibrin- exudation, heavy red lungs showing congestion and oedema (alveolar contain fluid and lined by hyaline membrane)
There is diffuse loss of surfactant -> alveolar atelectasis (collapse) -> lungs stiff and less compliant -> intrapulmonary shunt
Hard to manage on ventilator, always need to add positive pressure ventilation (PEEP)
